Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-9-13
pubmed:abstractText
In the polyclonal rat pancreatic beta-cell line INS-1, immunoreactive insulin (IRI, insulin and its precursors) and C-peptide (surrogate marker for mature insulin) were quantified after a 1-h incubation at 16.7 mM glucose with or without oleate. Oleate caused a 20% decrease (P <or= 0.01) and a shift towards mature insulin (P <or= 0.01) in intracellular IRI. As IRI secretion was significantly (P <or= 0.01) diminished in the presence of oleate at hyperglycemic conditions the loss of intracellular IRI had to be due to other reasons which was then examined by focussing on newly synthesized, radiolabelled IRI*. Thereby, oleate caused a 50% decrease in newly synthesized intracellular IRI* (P <or= 0.01) and-contrary to the findings in complete intracellular IRI-a shift towards immature insulin precursors. Taken together, exposure of INS-1 cells to oleate induces an intracellular lack of uncompletely processed IRI. This is due to an inhibited biosynthetic supply which can not compensate for intracellular IRI-degradation and (to a neglible extent) for insulin secretion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
287
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
397-401
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Intracellular depletion of insulin by oleate is due to an inhibited synthesis and not to an increased secretion.
pubmed:affiliation
Department of Internal Medicine I, University of Regensburg, 93042 Regensburg, Germany. cornelius.bollheimer@klinik.uni-regensburg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't